Nursing diagnosis of left ventricular failure in acute myocardial infarction

A new mode of therapy has recently been advocated for the treatment of left ventricular failure (LVF) due to acute myocardial infarction (AMI). This therapy involves the use of vasodilator drugs. Current literature places little emphasis on the clinical findings of the effects of vasodilators. This is especially true of nursing literature. Registered nurses (RN) in coronary care units (CCU) throughout the country are responsible for the monitoring and administration of vasodilator therapy. The majority of RNs use hemodynamic measurements as their only data to administer vasodilators. It is a well-known fact that electronic equipment utilized to obtain hemodynamic measurements can produce inaccurate data. Several medical studies exist which document the relationships between clinical findings and hemodynamic measurements during LVF due to AMI. Providing adequate care requires the RN to acquire appropriate skills and be capable of correlating these skills with all available data. The investigator theorized that a properly prepared RN could assess, diagnose and place patients, with LVF due to AMI, into clinical and hemodynamic subsets for purposes of management. A continuous measurement experimental design as described by Drew (1976) was utilized. The subject population consisted of 30 patients with AMI. The investigator utilized multiple assessments on each subject while providing a continuous measurement of the subjects'clinical progress throughout medical therapy. The majority of subjects (23) did not require hemodynamic monitoring. Correlation of clinical and hemodynamic subsets for those subjects who were monitored is not consistent. A significant percentage (26.6%,) of the subject population were less than 50 years of age. Therapeutic regimes could not be compared because of the physicians' reluctance to record appropriate data. Appropriately prepared RNs are capable of performing cardiovascular assessments while obtaining a sound clinical data base upon which to arrive at a nursing diagnosis. Utilizing the subset classification system, the RN could begin management of patients with LVF due to AMI on a regular basis. This may reduce the number of fatalities due to LVF.

NURSING DIAGNOSIS OF LEFT VENTRICULAR FAILURE IN ACUTE MYOCARDIAL INFARCTION by Alfred Bobby Miller A thesis submitted to the faculty of The University of Utah in partial fulfillment of the requirements for the degree of Master of Science College of Nursing The University of Utah December 1979 THE UNIVERSITY OF UTAH GRADUATE SCHOOL SUPERVISORY COMMITTEE APPROVAL of a thesis submitted by Alfred Bobby Miller I have read this thesis and have found it to be of satisfactory quality for a master's degree. f1ut ell 1f11 Dale i ! ) i /�/C' , Maeona K. ­ Jacobs (;� Chairman. Supervisory Commillcc I have read this thesis and have found it to be of �atisfactory quality for a master's . degree. PFM.7 Dale / /1 77 . d ,.. " '\ ' / / . . ' I Member, Supen isory A:', / v. . ' Commillcc ' . 4,' THE UNIVERSITY OF UTAH GRADUATE SCHOOL FINAL READING APPROVAL To the Graduate Council of The University of Utah: Alfred Bobby Miller I have read the thesis of in its f inal form and have found that (I) its format, citations, and bibliographic style are consistent and acceptable; (2) its illustrative materials including figures, tables, and charts are in place; and (3) the final manuscript is satisfactory to the Supervisory Committee and is ready for submission to the Graduate School. Dale Member. Supervisory Commiltee Approved for the Major Department . "" ) Approved for the Gradu3te Council ABSTRACT A new mode of therapy has recently been advocated for the treatment of left ventricular failure (L VF) due to acute myocardial infarction (AMI). This therapy involves the use of vasodilator drugs., Current literature places little emphasis on the clinical findings of the effects of vasodilators., This is especially true of nursing literatureo Registered nurses (RN) i.n coronary care units (CCU) throughout the country are responsible for the monitoring and administration of vasodilator therapy., The majority of RNs use hemodynamic measurements as their only data to administer vasodilators. It is a well-known fact that electronic equipment utilized to obtain hemodynamic measurements can produce inaccurate data., Several medical studies exist which document the relationships between clinical findings and hemodynamic measurements during L VF due to AML Providing adequate care requires the RN to acquire appropriate skills and be capable of correlating these skills with all available data" The investigator theorized that a properly prepared RN could assess, diagnose and place patients, with LVF due to AMI, into clinical and hemodynamic subsets for purposes of management., A continuous measurement experimental design as described by Drew (1976) was utilized., The subject population consisted of 30 patients with AMI. The investigator utilized multiple assessments on each subject while providing a continuous measurement of the subjects' clinical progress throughout medical therapy 0 The majority of subjects (23) did not require hemodynamic monitoring. Correlation of clinical and hemodynamic subsets for those subjects who were monitored is not consistenL A significant percentage (26.6%) of the subject population were less than 50 years of age 0 Therapeutic regimes could not be compared because of the physicians' reluctance to record appropriate data. Appropriately prepared RNs are capable of performing cardiovascular assessments while obtaining a sound clinical data base upon which to arrive at a nursing diagnosis. Utilizing the subset classification system, the RN could begin management of patients with LVF due to AMI on a regular basis. This may reduce the number of fatalities due to L VF v c TABLE OF CONTENTS Page ABSTRACT 0 ix • • • LIST OF TABLES . viii ACKNOWLEDGMENTS. • ix NURSING DIAGNOSIS OF LEFT VENTRICULAR FAILURE IN ACUTE MYCARDIAL INFAR CfION . .,. ,. ,. 1 2 Current Nur sing Practice,. . • • ,. . . LITERATURE REVIEW. .. . .. . • .. . 0 ,. ,. ,. ,. ,. ,. ,. 5 ,. Pathophysiological Considerations in Left Ventricular Thera PY Clinical Assessment of Cardiopulmonary Function.. Hemodynamic Monitoring of Cardiopulmonary Function,. Subset Classification and Hemodynamic. ,. • . . • ,. ,. Sodium Nitroprusside Therapy.. • . .. • • .. • . ,. .. • Conceptual Framework Statement of the Problem . . ,. • . ,. ,. Overall Purpose. ,. ,. ,. 0 • 0 • 0 0 • • .. • • • 0 0 " • 0 0 • 0 0 METHOD 0 0 0 • • 0 0 0 0 0 0 • "" 0 0 Q 0 • 0 0 0 ,. ,.,. 0 0 ,. ., 0 Results 0 0 0 0 0 0 c 0 Discussion.. ,. .. . . ,. ,. '" ,. 0 0 ,. • ,. ,. 0 ,. ,. 0 • ,. 0 • ,. 0 ,. ,. 0 ,. ... 0 ,. 0 ,. 0 0 0 ,. 0 0 • 0 ,. ,. 0 • ,. ,. ,. 26 27 0 Q 27 27 0 0 0 ,. 0 ,. ,. ,. . ,. 0' 0 Setting ,. Subject,. . ,. ,. • Design,. • Procedure. ,. . . ,. ,. • ,. ,. ,. . ,. • • . . • ,. ,. ,. RESULTS AND DISCUSSION ,. 5 11 12 13 16 18 24 • 0 0 • • 27 28 30 ,. 0 • 30 38 Appendices Page A. PHYSICIAN NOTIFICATION. • 43 B. PATIENT INFORMATION" " 44 C. CLINICAL ASSESSMENT. 0 0 • • • • 0 " D. HEMODYNAMIC MEASUREMENTS . • E 0 SUMMA R Y. • • " 0 • • • " • • 45 " • o 46 Q .. 47 F. OPERATIONAL DEFINITIONS. 77 BIBLIOGRAPHY. . • " " . . " " . " . 78 VITA . . • • . • . . " . " . " " . " . . . " . • • . 82 vii LIST OF TABLES Table 1. Page Characterization of Patients with Acute Myocardial Infarction Clinical Subset. . . . . " 0 20 It 0 0 0 0 0 0 31 0 0 0 0 0 0 0 0 32 0 0 0 0 0 0 !OJ 0 0 0 0 0 0 It 34 37 Comparison Matrix of Clinical and Hemodynamic Subset Classification 37 Classification of Hemodynamic Measurement by Range and Average. • 39 0 0 0 6. • Hemodynamic Subsets with Number of Hemodynamic Measurements . 0 50 0 Clinical Subjects with Number of Clinical Assessm. en ts 0 40 • Characterization of Patients with Acute Myocardial Infarction Hemodynamic Subset 0 30 0 0 • 0 0 0 0 0 0 0 0 0 0 0 • 0 • 0 0 0 0 0 0 0 • .. 0 • 0 0 0 0 0 0 0 0 0 • ACKNOWLEDGMENTS The investigator wishes to thank the supervisory committee members for their cooperation and patience during the development of this study 0 Particular appreciation of Ms 0 Liz Close, RN, MSN, and Dr. Steven Klausner, M .. D", for their efforts in the initial preparation and continuing development of the study is warranted. I also wish to thank my wife Margaret for her eternal patience, understanding and support during this study. NURSING DIAGNOSIS OF LEFT VENTRICULAR FAILURE IN ACUTE MYOCARDIAL INFARCTION A new mode of therapy has recently been advocated for the treatment of left ventricular failure (L VF) due to acute myocardial infarction (AMI). The new therapy involves after load reduction with the use of vasodilator drugs; the major drug utilized is sodium nitroprusside (SNP). Afterload is clinically defined as the resistance, or impedence, to ejection of the blood from the heart during systole 0 Current literature emphasizes the use of vasodilators, especially SNP(Awan, Vera, Demaria, Amsterdam & Mason, 1976; Chatterjee, Parmley, Ganz, Forrester, Walinsky, Crexells & Swan, 1973; Chiariello, Gold, Leinbach, Davis & Maroko, 1976; Cohn, 1973; Franciosa, Guiha, Limas, Rodriguera & Cohn, 1972; Guiha, Cohn, Mikulic, Franciosa & Limas, 1974; Moskowitz, 1975; Parmley, Chatterjee, Charuzi & Swan, 1974; Rowe & Henderson, 1974; Ziesche & FranciO,sa, 1977). Authors generally report hemodynamic effects of an increase in stroke volume. A decrease in pulmonary wedge pressure (PWP) contributes to increased cardiac output (CO), which together with an increase in stroke volume indicates improved left ventricular function. Sodium nitroprusside (SNP) has been in existence for many years and its hemodynamic effects were first reported by Johnson in 1929. Page~ Corcoran and Koppany began more intense research with SNP in 1955. As 2 modern technology progressed and more advanced pressure monitoring equipment became available, interest in SNP became increasingly intense, with a considerable number of studies being reported in the 1970' s . SNP therapy is now routinely prescribed by the physician with dosage dependent upon the desired hemodynamic responses 0 Little or no emphasis, to augment hemodynamic measurements, is placed on the physical assess ~ ment of the patient (Awan et a1o, 1976; Chatterjee et a1. ~ 1973; Chiariello et a1., 1976; Franciosa et a1., 1972; Guiha et a1o, 1974; Moskowitz, 1975; Parmley et a1., 1974; Rowe & Henderson, 1974; Ziesche & Franciosa, 1977). It has been the experience of this investigator that the registered nurse (RN) assigned to the coronary care unit is responsible for titrating SNP dosages to achieve the desired hemodynamic effects . Moskowitz (1975) also reports titration of SNP to be a regularly performed RN duty 0 Current Nursing Practice Throughout the country nursing is becoming increasingly involved in various treatment modalities.. In small community hospitals RNs do not have the benefit of full time physician coverage when monitoring patients with L VF due to AMI. The RNs generally responsible for SNP and other therapies have access to physicians on a limited basis. The RN therefore must correlate the hemodynamic measurements with the cardiovascular assessment to validate treatment effectiveness and achieve favorable therapeutic results. 3 In large medical centers where the RN may rely on house physicians to determine the course of therapy, the RN must still be capable of obtaining a clinical data base 0 Utilizing such data may alert the R N to a deterioration of the patient and provide a check on invasive moni ~ toring devices. This investigator has noted that often the RN uses only the hemodynamic measurements derived from arterial and balloon -tipped ·flotation catheters (Swan -Ganz) to evaluate the patiene s physiological response to ordered therapeutic modalities 0 It is unusual to observe an RN perform a cardiovascular assessment consisting of inspection, percussion' palpation and auscultation of the heart and lungs to determine if the clinical findings correlate with the findings of hemodynamic measure~ menta Current nursing education and literature provide the technique and methodology for performing cardiovascular assessment 0 This places the responsibility to perform assessments, on which therapeutic deci sions are based, within the domain of nursing practice (Adler, 1977; Delaney, 1975; Gordon, 1976; Mechner, 1976; Mechner, 1977; Silverman, 1971; Tanner, 1977). Current nursing literature does not, how ever, document the relationships between clinical findings and hemodynalnic measurements as do certain medical studies (Chatterjee & Parmley, 1977; Forrester, Diamond, Chatterjee & Swan, 1976; Forrester ~ Diamond & Swan, 1977). If the RN is to continue to accept responsibility for management 4 of complex therapy in patients with LVF due to AMI, then she must be capable of providing adequate care to the patient. This responsibility requires that the RN is able to: 1) perform a cardiovascular assessment, 2) utilize the assessment data and hemodynamic measurements to form a clinical data base, and 3) arrive at a therapeutic decision which is consistent with that of the physiciano LITERATURE REVIEW Pathophysiological Considerations in Left Ventricular Therapy Recent nursing literature discusses left ventricular failure (LVF), its pathophysiology and symptomology in a clear, concise manner (Foster, 1974; Tanner, 1977). Foster (1974) reports the effects of medications, electrolytes, endocrine disor.ders and autonomic nervous system disturbances on the failing heart. The major effects of medications on the heart are described as: 1) inotropic, 2) chronotropic, and 3) dromotropic; also, the author briefly discusses the cardiac effects of potentiation of one medication by another 0 Electrolyte imbalances may be caused by hypoxemia, acidosis, decreased serum calcium and decreased magnesium levels 0 These alterations give rise to arrhythmias and directly affect myocardial contractility 0 A notable omission from Foster's discussion of electrolyte imbalance is that of hypokalemia. This is a common electrolyte imbalance seen in patients treated with diuretics. This omission is readily corrected by the works of several other authors who fully discuss the difficulty (del Bueno, 1975; Haughey & Sica, 1977; Reed, 1978, pp. 84-85 and 87)0 Foster (1974) briefly discusses endocrine disorders such as: 1) hypothyroidism, 2) pheochromacytomas, and 3) adrenal crisis G Though the listed disorders are not discussed in 6 detail, they do provide incentive for a further review of literature. Foster (1974) discusses the role of the autonomic nervous system in detaiL Patients with severe pain as often experienced during AMI demonstrate evidence of vagal stimulation causing brachycardia and hypotension. Emotional responses such as anxiety produce enhanced sympathetic stimulation manifested by sinus tachycardia and a rise in blood pressure (BP) • The diagnostic methodology reported by Foster (1974) is applicable to this study and for usage by the nurse in the coronary care unit. Guidelines are provided for the purpose of performing a cardiovascular assessment allowing the RN to arrive at a reliable assessment of left ventricular function.. Emphasis for a nursing diagnosis is placed on: 1) history, 2) a physical assessment consisting of observable patient data, clinical examinations, laboratory findings, and 3) data from the physician's assess= ment.. The clinical evaluation is regarded as a continual and essential pro~" cess that is necessary to determine the patient's response to therapy" Tanner (1977) provides diagnostically useful information that is based on the symptomology observed in patients developing heart failure . Meltzer and Dunning (1972) report that heart failure is the major cause of death in patients admitted to coronary care units with AML The improvement in the nurse's ability to diagnose and treat death =producing arrhythmias is reported by Tanner (1977) to have eliminated arrhythmias as the major cause of death for patients with AMI who are hospitalized in ceus. The 7 author supports the concept that R Ns can also fulfill a similar role in reducing the number of deaths from heart failure. The RN, knowing that certain compensatory mechanisms occur following AMI, can assess and evaluate symptoms which are related to the compensatory mechanisms and the associated changes in cardiovascular hemodynamics 0 Tanner (1977) attributes the symptoms of heart failure to its effect on: 1) the heart itself, 2) the lungs, and 3) the degree of peripheral perfusion. For purposes of this discus sion, only the symptoms attributed to acute left ventricular failure will be considered" In discussing symptomology related to heart and blood vessel function Tanner (1977) begins with pathophysiological changes that occur within a short period of time following a decrease in cardiac output (CO). Stimulation of the sympathetic nervous system produces an increase in heart rate concurrent with inhibition of the parasympathetic nervous system" Initial autonomic activation results in an increase in CO 0 Tachy- cardia, defined as a persistent heart rate of greater than 100 beats per minute, as a symptom by itself is not evidence of L VF but may be due to increased sympathetic tone from other disease processes .. Pulsus alternans, one regular beat followed by a weaker beat during normal sinus rhythm, may occur in LVF and is due to variations in the strength of myocardial contraction with a decreased amount of blood being ejected during the weaker beat. Winthrobe (1974) reports that the weaker beat is probably the result of shorter myocardial fibers at the end of 8 diastole, therefore causing les s blood to be ejected during systole., Auscultation of the failing heart may reveal abnormal sounds, termed gallop sounds, which occur after the second normal heart sound (S2). The first gallop, S3' best heard over the apex of the heart, occurs early in diastole and is associated with the period of rapid ventricular filling. Its presence indicates a relative increase in the volume of blood that is being injected into the left ventricle (volume overload). Another gallop sound, S4' is heard during ventricular filling toward the end of diastole. This sound is believed to be caused by decreased compliance of the left ventricular wall due to ischemia. A combination of both S3 and S4 sounds is termed a summation gallop and may occur during tachycardia when diastole is shortened and the two sounds merge., Dilation and hypertrophy of the heart may result if the myocardium cannot eject the entire volume of blood from the left ventricle during systole According to the Frank-Starling Law, the greater the end diastolic volume~ the stronger the contraction of the myocardial fiber within limits The fail = <> 0 ing heart will compensate by this method to a maximum sacromere length of 2.2 microns. Once this point is reached, the heart cannot distend further to increase its stroke volume. Prolongation of this compensatory mechanism results in irreversible cardiac dilatation" The heart can also increase its muscle mass and hyperthrophy to compensate for a decreased stroke volume Q Clinical assessments to determine hypertrophy and dilatation are the point of maximum impulse (PMI), the chest X -ray and the electrocardiogram" 9 Although Tanner (1977) discusses clinical findings common to the respiratory system that occur with LVF, West (1974) gives a more concise report.. West (1974) states that an increase in end diastolic volume causes an increase in left ventricular pressures which in turn causes the pressure in the left atrium and pulmonary veins to elevate" As a result, pressures in the pulmonary capillaries exceed critical levels and fluid croses the alveolar epithelium into the alveolar spaces, causing pulmonary edema" This may occur when the pressure in the pulmonary capillaries exceeds 25 mm Hg" Pulmonary edema may be seen on chest X -ray with rales heard as a late sign" Depending upon the amount of fluid involved, increasing dullness to percussion can be utilized to outline areas of fluid in the lungs or periphery. If an individual has been bedridden for several days, rales may be due to the pooling of fluids at the bases of the lungs because of inactivity. Rales due to pulmonary congestion of a cardiac origin are usually heard in the lung bases initially and are defined as fine and crepitant. The auscultated height of the rales in the lungs may correlate with the severity of the congestion" Another early symptom related to pulmonary venous congestion and elevated left ventricular filling pressure is difficult or labored breath = ing" This usually manifests initially only upon exertion and eventually as the pulmonary congestion increases, it is present even at rest.. Orthopnea also occurs during acute, LVF and it is thought to be caused by the follow~ ing mechanism.. While a person is upright, blood is pooled in the lower 10 extremities because of gravitational forces and upon reclining, pooled blood returns to the right heart, effectively increasing the circulating blood volume. With increased blood volume» intravascular pressure rises which can subsequently lead to more fluid being forced into the interstitial spaces of the lung, causing decreased distensibility of the lung with increased difficulty in breathing Coughing» another diagnostic clue 0 reported by West (1974) usually starts as dry and nonproductive and progresses to productive hemoptysis as hydrostatic pressures in the pulmonary capillaries become great enough to rupture blood vessels 0 Depending upon the fragility of the blood vessels hemoptysis may occur with hydrostatic pressures in excess of 28 mm Hg (West, 1974). Various other symptoms are associated with LVF 0 Many commonly seen symptoms are due to a decreased CD and blood flow to vital organs. Tanner (1977) reports cheyne-stokes respirations, manifest by alternating periods of hypo and hyper ventilation, may occur as a late symptom of LVF ~ Guyton (1976) states that the mechanism of causation is disordered cyclic changes in the oxygen (02) and carbon dioxide (C02) tensions in arterial blood initiated by a low CO2 , Such variable 02 and CO levels may be due 2 to decreased circulation times decreased blood pressure, Q Clinical signs and symptoms such as fatigue~ weakness, restlessness and oliguria are also evidenced in acute phases of L VF 0 As stated earlier, a fall in CO stimulates the sympathetic nervous system 0 Tanner (1977) reports that in the kidney this results in 11 constriction of afferent arterioles.. A decrease in the glomerular filtration rate results in diminished urine output 0 The decreased blood flow to the kidney activates the renin-angiotensin cycle. Angiotensin, a potent vasoconstrictor, causes further reduction in renal blood flow 0 The author states that the signs of fatigue, weakness and restlessness are probably due to the decreased blood flow to the skeletal muscles e Tanner (1977) addressed the most common symptoms seen with LVF. The presentation is logical, easily understood, and includes some pathophys iology as sociated with L VF. The di scussion provides incentive for further study of advanced literature so that LVF may be thoroughly understood and appropriately managed .. Clinical Assessment of Cardiopulmonary Function Silverman (1971) reported a program directed at increasing the registered nurse's (R N) ability to obtain a clinical data base consisting of a detailed history and a cardiovascular examinationo The information obtained was recorded in the patient's chart, using the problem ~oriented method . The purpose of the program reported by Silverman was to provide a broader data base to enable the physician to follow the patient's progress throughout each shift. Comparisons could also be made by the nurse to assess the patient's progress on succeeding shifts .. Silverman (1971) reported that some physicians initially respond to the project with reluctance because the clinical findings and charting were done on the Physician's Note section 12 of the patient's chart. According to Silverman (1971, po 380), an extensive backgroupd in anatomy , physiology, pathophysiology, electTocardiography, clinical pharmacology and physical diagnosis enabled the nurse to perform a complete and accurate cardiopulmonary assessment. Several advantages to nursing involvement in the constant and. in -depth management of patients are apparent: 1) a sound basis for evaluation of nursing care is provided in the charted records, 2) immediate identification of problems in educational preparation or misinterpretation of data is possible which allows for corrective feedback, and 3) a source of highly reliable physiological data is readily available to the physician (Silverman, 1971) 0 A conspicuous omission in the Silverman (1971) report was that the author did not convey whether nurses were included in the decision making process of formulating a plan for therapy 0 The RNs were trained and utilized to gather and report data utilized to gather and report data utilized by the physician, however? no other involvement of the RN is reportedo Hemodynamic Monitoring of Cardiopulmonary Function Hemodynamic monitoring of patients with left ventricular failure (LVF) associated with AMI became common practice only in the 1970so Many studies (Awan et ala ~ 1976; Chatterjee et ala? 1972; Chiariello et aL, 1976; Cohn, 1973; Franciosa et aL, 1972; Parmley et {iI., 1974; Rowe & Henderson, 1974; Ziesche & Franciosa, 1977) have been conducted 13 utilizing the balloon -tipped flow directed catheter (Swan -Ganz) and recording devices to describe the effects of various medications on the hemodynamics of the cardiopulmonary system. The primary focus of these studies has been to manipulate the pulmonary artery pressure (PAP), pulmonary wedge pressure (PWP), cardiac output (CO) and cardiac index (CI) ~ The authors generally agree that these parameters can be desirably altered with the use of vasodilator therapy ~ and for patients experiencing acute LVF associated with AMI, desired values for the PWP are commonly between 15-18 mm Hg. with the CI greater than 2.2 l/min/m2 (Forrester et al o , 1976, 1977). The major criticism of these studies is that they are hemodynamically oriented while providing the reader with little or no clinical findings which may be useful to assess the hemodynamic response obtained. Subset Classification: Clinical and Hemodynamic As nursing becomes more sophisticated, professional nurses are seeking greater responsibilities 0 Gordon (1976) describes nursing diagnosis as: Description of actual or potential health problems, which nurses, by virtue of their education and experience, are capable and licensed to treaL (po 1299) The registered nurse who functions in the role of diagnostician must be knowledgeable of the physiologic reasons for clinical symptoms usually seen following acute myocardial infarction and must be knowledgeable 14 the hemodynamic response of the cardiovascular system 0 Gordon (1976) states that the end product of nursing diagnosis is the placement of the patient in one or more diagnostic categories for the purpose of determining therapy. She did not attempt to broaden this concept into specific specialty fields of nursing. Several studies have attempted to classify the degree of loss of LVF in AMI on the basis of clinical and hemodynamic parameters (Chatterjee & Parmley, 1977; Forrester et al.q 1976, 1977) 0 The patients in such studies were clinically categorized on the basis of physical assessment and invasive hemodynamic measurements 0 Forrester et al. (1976, 1977) categortzed the hemodynamic responses and clinical findings commonly found in patients experiencihg AML In Forrester's et a1.. (1977) scheme, both hemodynamic and clinical findings are divided into four subsets with a parallel relationship existing between the corresponding subseL A sample of the classification system as utilized by Forrester et a10 (1977, po 139) is as follows~ Subsets Cli.nical Hem odynam ic HI) PWP less than 18 mm Hg and CI greater than 2 02 l/min/m2 0 Cl) No pulmonary congestion or peripheral hypoperfusion H2) PWP greater than 18 mm Hg. C2) Pulmonary congestion present H3) CI less than 202 l/min/m2 C3) Peripheral hypoperfusion present 15 H4) PWP greater than 18 mm Hg and CI less than 2.2 1/min/m2 0 C4) Both pulmonary congestion and peripheral hypoperfusion present The study by Chatterjee and Parmley (1977) does not include subsets equivalent to the clinical and hemodynamic classifications of Forrester et a10 (1977). Forrester et a10 (1977~ p. 137) report that by utilizing their classification system, patterns may be established which aid in the prognosis and treatment following AMI. The authors further report that even with accurate equipment nothing can substitute for the bedside cHnical examination. Forrester et a1. (1977) with the use of clinical subsets, were able to predict the hemodynamic subset with approximately 83% accuracy. This means that 83% of the time the actual hemodynamic measurement corresponded with that predicted by the clinical finding" Terms for the study used in the clinical subset classification scheme were carefully defined" Peripheral hypoperfusion was defined as the presence of: 1) decreased skin temperature, 2) mental confusion, and 3) oliguria in conjunction with arterial hypoperfusion or sinus tachycardia with the patient breathing room air before sedation. Mental state p skin temperature and color were determined subjectively. Oliguria was defined as urine output of less than 40 cc/hr" Arterial hypoperfusion was indicated if the systolic blood pressure was less than 100 mm Hg and sinus 0 tachycardia was defined as a heart rate of more than 125 beats/minute. Pulmonary congestion was considered present if auscultatory findings 16 revealed rales over the posteriobasal chest and radiographic findings were positive for pulmonary congestiono Forrester et aL (1977) also discuss several classes of medications utilized for therapy in patients and identify their effects on CO and PWP o The hemodynamic effects of the drug classes are as follows: Class CO Inotropics Diuretics Vasodilators Beta -adrenegic blockers PWP Unchanged or Increased Unchanged or Decreased Unchanged Decreased Increased Decreased Decreased Unchanged or Increased Utilizing the above guidelines, medical therapy was tailored to the patient's subset classification 0 For example, if a patient is assigned to clinical subset C4 and hemodynamic subset H4, the patient will have a decreased CI and an increased PWP Q Vasodilators would be the medication of choice as these medications increase CD and decrease PWP 0 The author s contend that in patients with AMI, prime consideration should be given to correcting the abnormal hemodynamics Q The studies by Forrester et aL (1976, 1977) are complete when considering the factors of hypoperfusion and pulmonary congestiono These studies demonstrate that it is possible to interrelate clinical findings and hemodynamic responses in patients with L VF due to AML Sodium Nitropruss ide Therapy It has been this investigator i s experience that the major vasod)l 17 currently used in the treatment of LVF associated with AMI is sodium nitroprusside (SNP). Of the many studies related to the use of vasodi1ators two are of prime importance to the nursing management of SNP therapy 0 Moskowitz (1975) discusses vasodilator therapy in general with a specific section related to SNP.. The author reports hemodynamic changes associated with SNP therapy as increased CO and decreased PWP 0 Infor- mation relevant to nursing implications contributed by Moskowitz are: 1) an emphasis for careful history taking, 2) the need for continuous monitoring of hemodynamics to maintain the PWP between 15 -18 mg Hgo without inducing hypotension, 3) patient activities that may potentiate the effects of SNP, and 4) precautions utilized in preparation of SNP for intra venous infusion. Unfortunately, the report is not primarily concerned with associated changes in the clinical findings and is therefore narrow in scope 0 Ziesche and Franciosa (1977) in their article also do not provi.de the reader with useful clinical data by which to assess SNP therapy. Their major contribution is concerned with the administration of SNP. They provide information in a clear concise manner which enables the reader to understand the administration and evaluation of SNP utilizing hemodynamic measurements.. Included in their report is a cornplete reference table for the titration scheduling of SNP dosage (Ziesche & Franciosa, 1977, p. 101)0 18 The literature on left ventricular failure and SNP therapy reveals that a core of valuable information is available to the RN involved in the care and management of the patient with LVF associated with AMI. Clinical data may be utilized as the RN desires, however ~ it has been the experience of this investigator that the majority of RNs use only bits and pieces of clinical informationo An extensive review of literature revealed no centralized, succinct report on the synthesis of clinical and hemodynamic data designed for and by RNs. Thus~ it may be diffi- cult to arrive at a nursing diagnosis and determine appropriate therapy for patients undergoing treatment of LVF due to AMI. Although most of the available literature on clinical and hemodynamic responses to vasodilator therapy is physician oriented, it can be understood by the professional nurse 0 By synthesiz ing information con ~ cerning the pathophysiology of AMI, clinical signs and symptoms of LVF and the involved hemodynamics, the professional nurse can arrive at a nursing diagnosis 0 Utilizing a classification system such as that pre = pared by Forrester et al. (1977) the RN could manage patients with L VF associated with AMI within more complete parameters 0 Conceptual Framework The professional registered nurse must possess an adequate understanding of the relationship between clinical findings and the hemodynamic function of the myocardium to adequately assess the pathophysiology of 19 acute myocardial infarction. The RN must also possess understanding of the physiological effects of vasodilators on this relationship. The following discussion is based on the model in Figure 1 designed by the investigator which depicts a relationship between key factors associated with vasodilator therapy and management 0 The arrows serve as a guide to direct the reviewer's attention toward the clinical and hemodynamic aspects of the pathophysiology that occurs during AMI, L VF and vasodilator therapy. The relationships within the model have been explained in the review of literature. Each of the four parts of Figure 1 relate to one of the four clinical and hemodynamic subsets suggested by Forrester et a 1. (1 977) • The clinical findings and hemodynamic alterations associated with acute myocardial infarction (AMI) are attributed to the extent of myocardial damage during the infarction process (Netter~ 1974)0 The patient with an uncomplicated AMI (see Figure I-A) may exhibit few or no abnormal clinical findings from the infarction process" SNP reduces the impedence against which the heart must eject blood during systole.. This results in a larger volume of blood ejected without an increase in myocardial workload (see Figure 1 =D)~ therefore, myo= cardial oxygen consumption remains the same or improves due to reduced workload. This decreases the possibility of injury or necrosis to the myocardium adjacent to the infarction site in the ventricle (Armstrong~ Walker, Burton & Parker, 1975; Chatterjee et aL, 1973; Chiariello et aL, 1976; 20 < > HI) PWP I8mm Hgo -(; CI 202 I/min/m2 Classification: ,... CI) No complications ~ HI) Hemodynamic mea- ~CI) surements of: 1) PWP I8mm Hg. 2) CI 202 I/min/m2 Assessment: < > No pulmonar y congestion or peri phera 1 hypo~' perfusion present t l HI) Monitor for digression+> CI) Assess for di= to other subsets gres sion to other subsets Therapy: PWP - Pulmonary Wedge Pres sure CI - Cardiac Index CXR - Chest X-Ray M - Murmur AMI - Acute Myocardial Infarction Legend: Figure 1 =A 1 0 AMI g Hemodynamic Alterations (H) and Clinical Findings (C) 21 Classification: Assessment: H2) PWP >18mm Hg 0 lIII(;oo(;~-7""> C2) Pulmonary co nge s - tion present 1 > H2) PWP 18mm Hg ,II(; when hemodynamic measurements completed 0 .... C2) 1 0 2" 3" 40 Therapy: H2) Diuretics to in crease or stabilize CO 011( .. C2) 1 Rales~ rhonchi or wheezes present CXR positive for interstitial or alveoli pulmonary edema S3' S4' and M may be present Respirations may be slow & deep or rapid & shallow Rales, rhonchi or wheezes may decrease 2" CXR shows decrease in interstitial or alveolar pulmonary edema 30 S3~ S4 and M may decrease until gone 40 Respirations may return toward nor mal rate and depth Q Legend: PWP - Pulmonary Wedge Pressure CI - Cardiac Index CXR - Chest X -Ray M Murmur AMI - Acute Mycardial Infarction Figure I-Bo AMI~ Hemodynamic Alterations (H) and Clinical Findings (C) 22 <2.2 1/min/m2 ~ C3) Classification: H3) CI Peripheral hypoperfusion present Assessment: H3) CI< 2,,2 1/min/m2 ~ C3) 1" Decrease in urine when hemodynamic output measurements com ~ 2" Skin: cool, clammy pleted 3" Mental obtundation may be present 4. Hypotension systolic 100mm Hg" t 1 Therapy: H3) Inotropic Agents to ~ C3) 1.. Skin may be warm/ 1" Increase or dry stabilize CO 2.. Mental state returns 2. Decrease or toward normal stabilize PWP 3" Urine output exceeds 3.. Volume replace40 ml/hr. when averaged over 24 ment to possibly increase PWP and hr .. period 4.. Systolic BP increase CO if PWP is norto greater than 100 mal or low and mm Hg. CO is decreased Legend: PWP - Pulmonary Wedge Pressure CI ~ Cardiac Index CXR - Chest X-Ray M - Murmur AMI - Acute Myocardial Infarction Figure I-C. AMI, Hemodynamic Alterations (H) and Clinical Findings (C) 23 Classification: > H4) PWP 18mm Hg.. C4) Both pulmonary conCI 2.2 1/min/m2 ~ gestion and peripheral hypoperfusion present < J Assessment: > < J H4) PWP 18mm Hg. ~ C4) 10 Rales, rhonchi, and CI 2.2 1/min/m2 wheezes may be when hemodynamic present measurements are 20 CXR positive for completed effusions or other signs of pulmonary 3 0 S3' S4 or M may be present 40 Respirations may be slow & deep or rapid & shallow 5" Decrease in urine output 6 0 Skin: cool, clammy 7.. Mental obtundation ma y be present H4) Vasodilators and ~ diuretics to: 10 decrease PWP toward normal 2. Increase CIabove 202 1/min/m2 3.. Inotropic agents may be utilized to increase BP caus ing increased perfusion to vital organs ~ C4) 1 . Rales, rhonci, wheezes begin to appear 2.. CXR shows decrease of effusions/ ederna 3. S3~ S4 and M begin to disappear 4. Respirations return toward normal rate and depth 5.. Urine output in = creases to 40 ml/hr x 24 hr. period Legend: PWP ~ Pulmonary Wedge Pressure CI - Cardiac Index CXR - Chest X -Ray M - Murmur AMI - Acute Myocardial Infarction Therapy: Figure I-D. AMI, Hemodynamic Alterations (H) and Clinical Findings (C) 24 Cohn, 1973; DaLuz, Forrester & Wyatt, 1975; Franciosa et aI., 1972; Guiha et al., 1974; Parmley et aI., 1974; Rowe & Henderson, 1974; Schlant, Tsagaris & Robertson, 1962; Ziesche & Franciosa, 1977) 0 As a result of the increased CO several clinical findings can be expected to occur (see Figure 1-D)o Depending upon the patient response to SNP, therapy may be dramatic and occur within minutes 0 The blood pressure may remain the same, decrease or increase slightly. Heart sounds such as S3 and S4 may gradually disappear because the ventricle may become less distended and arterial filling may not be as rapid. There will be less hydrostatic pressure exerted on the pulmonary circulation because of increased CD. Rales may begin to disappear and pulmonary congestion will decrease, allowing respirations to slow and become less difficult (Forrester et al., 1976, 1977; Foster, 1974; Tanner, 1977)0 The effects of SNP therapy are closely related and dependent upon the physiological state of the myocardium 0 Titration of SNP to produce the desired effects and improve the physiological state is variable 0 SNP therapy is a dynamic treatment mitigated by concomitant clinical findings and hemodynamic responses 0 Statement of the Problem The registered nurse (RN) in the coronary care unit (CCU) is responsible for constant physiological and electrocardiographic monitoring of the patient who has incurred an acute myocardial infarction (AMI) ~ 25 Physiological monitoring includes responses to various therapeutic regimes Q A survey of 22 medical records of patients with AMI for episodes of hypoperfusion and pulmonary congestion (as defined by Forrester et alo, 1976, 1977) which involved hundreds of entries on nursing and progress notes, revealed that the majority of R Ns do not record their clinical findings 0 Of approximately 50 episodes of hypoperfusion and pulmonary congestion, verified by recorded hemodynamic measurements, only six assessments of the cardiopulmonary system were recorded. In general, it was not unusual to find recorded increases in the pulmonary wedge pressure (PWP) from 15 mm Hg. to 30 mm Hg. or greater in less than 2 -3 hours. The RN caring for the patient continued to increase the SNP infusion rate without reporting the findings of a clinical assessment which would substantiate the l1emodynamic measurements .. Fallibility of electronic equipment utilized in hemodynamic moni ~ toring is well acknowledged (Adams, 1976; Forrester et aL, 1977; LalU, 1978; Woods, 1976). This investigator, in agreement with others (Adams 1976; Lalli, 1978· Woods, 1976), have found the cause of inaccuracy to be mainly due to improper calibration of the monitoring equipment .. Forrester et ala (1977) indicates that although hemodynamic monitoring may be accurate, nothing substitutes for the bedside clinica1 assessment and its findings 0 If the RN is to continue to be responsible for immediate care of the AMI patient and the administration of medical therapeutic regimes, she must be capable of performing a physical assessment of 9 26 the cardiopulmonary system. This is particularly important when SNP or vasodilators are administered 0 Correlation of clinical findings to the hemodynamic measurement is essential for safe care 0 Review of nursing and progress notes by this investigator revealed that the RN is either: 1) unwilling to obtain or record data of physical findings, or 2) not able to correlate clinical findings with hemodynamic measurements. Overall Purpose The purpose of the study is to determine if the registered professional nurse who has successfully completed an approved course of study consisting of cardiovascular anatomy, physiology, pathophysiology, electrocardiography, cardiac pharmacology and physical diagnosis can in accordance with Forrester's et al. (1977) subset classification parameters: 1. Utilize an obtained clinical data base to determine the appro = priate clinical subset for each subjecL 2. Utilize known hemodynamic measurements to determine the appropriate hemodynamic subset for each subject. 30 Determine a therapeutic regime which would approximate that of the physician. METHOD Setting This study was conducted in the coronary care unit (CCU) of a 580bed hospital in Salt Lake City, Utah 0 The CCU has a total of 12 beds. All beds can be monitored from the central nursing station for arrhythmias 0 The nursing care for all subjects was provided by the staff of the CCU. Subjects The sample of 30 subjects was selected from the population of all patients admitted to the coronary care unit, arriving in a predetermined time period, who exhibited electrocardiographic and serum changes consis tent with acute myocardial infarction. Exclusions included: 1) Those declining to participate in the study. 2) Those already receiving SNP therapy 0 Design This study is an exploratory continuous measurement research design as described by Drew (1976, p. 37) 0 It does not meet the criteria of baseline or multibaseline designs because treatment is begun immedi c~ ately which precludes the establishment of baseline data. 28 Procedure Consent Within 48 hours following admission the patient was interviewed to obtain consent. If the patient was not capable of giving an informed consent, his/her immediate family was contacted to provide consent for participation in the study. Attending physicians were contacted regarding each subject and cooperation obtained (see Appendix A). Medical History and Assessment After the consent had been obtained and the physician informed, a detailed history was obtained by the investigator. Emphasis was placed on cardiopulmonary factors" Following the history, the investigator performed a cardiopulmonaryassessment, using the physical examination techniques and procedures advocated by Alder (1977) and other authorities (DeGowin & DeGowin, 1976; Judge & Zuidema, 1968; Mechner, 1976, 1977; Prior & Silverstein, 1973) A minimum of three cardiopulmonary assessments, performed at approximately 24-hour intervals, were completed by the investigator for each subjecto Two subjects expired before this procedure could be completed 0 Hemodynamic Measurements Each hemodynamically monitored subject was connected to the following equipment: a) Bently Manufacturing Company Model 800 29 Transducter, b) Gould Manufacturing Company Brush Recorder Model 2200, c) Hewlett-Packard bedside and central monitoring oscilloscopes, d) General Data Corporation Model 3300 computer with Hewlett-Packard terminal oscilloscope.. Hemodynamic measurements were made by the CCU staff nurses using unit procedures 0 The investigator performed a cardiopulmonary assessment in immediate conj unction with hemodynamic measurements recorded during the study. Data Acquisition All data was recorded on the appropriate collection forms (see Appendices A, B, C, D, E). The investigator utilizing staff and self gathered data, assigned the subject to clinical and hemodynamic subsets" The investigator then developed a therapeutic regime and following each cardiopulmonary assessment recorded his findings on the Patient Assessment Form (see Appendix C). If the physician had completed an assessment within three to four hours of the investigator's assessment a comparison of the investigator's therapeutic regime and the physician's regime was made by the investigator. This comparison was also recorded on the appropriate form (see Appendix D). All data was summarized by the investigator on the Summary Form (see Appendix E) g RESULTS AND DISCUSSION Results Statistics The descriptive nature of this study necessitated measures of central tendency, mean and standard deviation be utilized. Raw score and percentiles were utilized to describe the subject's assignment to subset cIa s sifica tion. Findings Clinical Subsets. Table 1 describes the common characteristics of all 30 subjects assigned to clinical subsets developed by Forrester et al. (1976, 1977). Assignment to clinical subsets is as follows: 1) Cl no pulmonary congestion or peripheral hypoperfusion, 2) C2 pulmonary congestion present, 3) C3 peripheral hypoperfusion present, 4) C4 both pulmonary con gestion and peripheral hypoperfusion present. The majority (63%) of the subjects were assigned to Cl. This is consistent with previous experience of the investigator 0 Forrester et al. (1977) also report that the majority of subjects fall into this subseL The authors fail to report, however, if more than one assessment was done on each subject. The ages of subjects classified in clinical subsets ranged between 35-81 years, the mean age was 60-62 years. This is consistent with data 31 Table 1 Characterization of Patients with Acute Myocardial Infarction Clinical Subset I Patients Age: Range Mean Standard Division 19 II III IV S 3 43~SO Total 30 35-S1 60.S9 7.S 62.62 7.9 46-74 60.23 7.7 Female Male 2 17 1 7 1 2 4 26 History: Previous MI Previous CHF 3 2 2 2 1 7 Sex: 3 CHF - Congestive Heart Failure MI - Myocardial Infarction reported by Forrester et ale (1977). A clinically significant percentage (26.6%,) of the subjects were under 50 years of age. Forrester et al. (1977) did not report this parameter. The study population included four subjects (13.3%,). This differs from the percentage of 21.5% as reported by Forrester et aL (1977, Table I, p. 13S). The larger population or the time frame of the study reported by Forrester et al. (1977) may account for this difference. Patient histories reveal only seven subjects (23. 3%,) with previous infarctions and three subjects (10%,) with a previous history of congestive heart failure. 32 Hemodynamic Subsets. During the study period only seven subjects were hemodynamically monitored Table 2 describes the cornmon charac- 0 teristics of these subjects assigned to hemodynamic subsets The hemo- 0 dynamic measurements, obtained by staff RNs assigned to the CCU so that internal bias would not skew findings, were used to assign patients to a particular subset as outlined in Figure 1. The hemodynamic subsets are defined as follows: 1) HI normal hemodyanmic measurements, 2) H2 puI= monary wedge pressure (PWP) greater than 18 mm Hg., 3) H3 a cardiac index (CI) of less than 2.2 l/min/m2. The ages of subjects classified in hemodynamic subsets ranged between 43-76 years, the mean age was 55-61 years . This is consistent with Forrester et ala (1977). A clinically significant percentage (42.85%) Table 2 Characterization of Patients with Acute Mycardial Infarction Hemodynamic Subset Patients Age: Range Mean Standard Deviation Sex: Female Male History: I II III IV Total 1 2 1 3 7 59 59 1 Previous MI Previous CHF 43-76 59.5 5.45 1 1 1 61 61 44=75 55 4 .. 28 1 1 2 2 5 1 '--CHF - Congestive Heart Failure MI - Mycardial Infarction 33 were under 50 years of age. There were two female subjects (28.5%). Only one subject (14.2%) reported a previous history of congestive heart failure and none had a previous history of AMI. This sample is too small to compare with Forrester et al. (1977). Clinical Subjects. Table 3 represents the categorized results of clinical assessments completed by this investigator. Since no study could be found which reports multiple assessment and placement into clinical subsets as defined by Forrester et al. (1977) the percentages reported by the investigator cannot be compared with other findings at this time. Because of the large number of clinical assessments accomplished (137) a compari~ son was made with Forrester et ale (1977) data (see Figure 2). The most striking difference occurs when comparing clinical subset C4. Approximately 10.2% of the assessments completed by the investigator placed subjects into category C4. Forres ter et ala (1977) report approxi ~ mately 33.5% in this subseL Clinical subset C3 is another area of striking difference, with this investigator reporting 2.189% of the assessments in this category. Forrester et al. (1977) report approximately 1005% in clinical subset C3. These differences may be attri.buted to the lack of high acuity subjects available during this study. Also, Forrester et ala (1977) report their study was approximately 5 years in length. The large time difference may have allowed Forrester et al. (1977) to be more selective and choose only patients with expected high acuities. Other factors such as different medical regimes or the time frame before 34 Table 3 Clinical Subjects with Number of Clinical Assessments Subjects # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 Total I Subsets III II IV Total Assessments 3 3 3 3 3 4 4 1 3 4 4 1 8 9 5 5 3 4 6 3 3 6 5 5 3 4 3 3 8 1 1 1 1 2 3 2 5 4 3 1 1. 1 1 5 4 4 1 1 2 4 2 4 2 10 5 1 2 72 48 3 2 5 4 5 2 9 4 4 5 4 3 11 3 5 7 5 3 14 137 35 initiation of therapy may have also contributed to this difference. Due to a lack of data these factors cannot be evaluated. It can be reported that the investigator's clinical as ses sments concluded the maj ority (52.5%) of the subjects were placed in clinical subset Cl, no complications. Forrester et al. (1977) report approximately 37% in this category. This data clinically supports the contention that Forrester et ale (1977) had access to patients with higher acuities. 100 90 - 80 ~ rJ) ~ ~ Q) 70 ~ 8 rJ) rJ) Q) rJ) rJ) ~ 60 50 "H 0 H Q) 40 ..0 8 ::l Z ' -.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. 30 20 10 '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. Cl - "" "" '-... '-.. --- ......... '-.. '-.. '-.. '-.. '-.. ........... '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. C2 ~ '-.. =:t rG. Miller Study Legend II/ IIII Forrester et ale (1977) Figure 2. Comparison of Clinical Subjects '-.. '-.. '-.. ~ '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. r - '-.. '-.. '-.. '-.. '-.. 1::::-- C4 36 Hemodynamic Subjects. Only seven subjects required hemodynamic monitoring during the study, however, initial planning required ten subjects in this category., The sporadic occurrence of these subjects rendered it impossible to obtain the required data. By using multiple hemodynamic assessments it was possible to accomplish 33 assessments on the 7 subjects obtained., If a single assessment had been clinically significant number for analYSiS" made~ 7 would not constitute a Multiple assessments also allowed the investigator to assess the subject over the acute phase of the medical regime. When compared with Forrester et al. (1977), who accomplished only one assessment per subject, this produces a more clinically significant evaluation of the medical regime. By utilizing multiple assessments the 33 assessments obtained would be significant for clinical analysis. Table 4 summarizes the placement of subjects within the four hemodynamic subsets. The difference in numbers of the hemodynamic measurements between the two studies (33 vs. 200) does not allow for statistical comparison. This investigator reports a relatively even distribution of subjects within the hemodynamic subset classification system. Table 5 demonstrates a comparison of the clinical and hemodynamic subsets of all subjects who were hemodynamically monitored. The clinica 1 subset did not correlate with the hemodynamic subset on 19 comparisons (57%). The discrepancy in correlation between clini.cal and hemodynamic subset classification is due in large part to the MPWP which were less 37 Table 4 Hemodynamic Subsets with Number of Hemodynamic Measurements Subsets I Total Assessments II III IV 14 1 1 2 4 17 1 1 2 Patient # 22 3 24 2 1 5 9 2 26 4 2 2 28 30 Total 9 7 4 1 2 7 1 4 5 8 9 33 Table 5 Cornparison Matrix of Clinical and Hemodynamic Subset Classification Hemodl:namic Subsets Clinical Subsets I 1 II 19 I 7 II III IV Total Assessments 1 2 8 1 3 38 1 7 5 26 9 8 9 66 III IV Total 13 33 7 38 than 18mm Hg in 13 comparisons. Table 6 classifies the raw data secured from subjects who were hemodynamically monitored. It displays the range and average of the cardiac index (CI) and the mean pulmonary wedge pressure (MPWP). This data indicates that hemodynamic monitoring was appropriate in all but one subject. Raw data for all subjects from which subset classifications were made is displayed in Appendix E. Progress Notes. Physician Progress Notes were reviewed for the following data: 1) time of day, 2) recording of hemodynamic measurements, 3) clinical findings, and 4) planned therapeutic regimes. Progress notes for comparison purposes, were deficient in three areas: 1) they consistently failed to provide the time of clinical assessment, 2) hemodynamic measurements were recorded on only 2 occasions, and 3) a recorded planned therapeutic regime was not consistently available. Thus, it was not possible to perform a significant comparison of the investigator's therapeutic regime with that of the physicians. Discussion Since no study utilizing mUltiple clinical assessments of subjects who have developed left ventricular failure due to acute myocardial infarction with subsequent assignment to clinical and hemodynamic subsets could be found, this study could not be compared with similar studies 0 39 Table 6 Classification of Hemodynamic Measurements by Range and Average Patient # CI (L/min/m2) MPWP (mm Hg) Total Measurements 14 Range Average 1 .. 79-2.15 1.99 13-26 21025 4 17 Range Average 2.03-2.54 2.28 20-22 21 2 22 Range Average 1.83 -2 .56 2.116 12-16 14.25 9 24 Range Average 2.65-2.75 2.7 14 ... 15 14.5 2 26 Range Average 2.45-206 2.51 19-25 22 4 28 Range Average 1.6-2022 2.1 12-27 20.14 7 30 Range Average 1014-2.02 106 15-21 19 5 Range Average 1.14-2.75 2.11 12-27 18.63 33 Summary 40 Limitations Certain aspects of the study posed limitations that had not been anticipated. The time frame for the study did not allow a large patient population. The methodology for performing hemodynamic measurements was not controlled. In an attempt to limit internal bias, the investigator decided it would be more appropriate not to know the hemodynamic measurements prior to completing a cardiopulmonary assessmenL This placed the responsibility for hemodynamic measurements upon the nursing staff of the CCU. It was subsequently determined that each RN did not accomplish the hemodynamic measurements with the same technique. For example, some R Ns did not calibrate the transducer at each measure ~ menL This may have introduced error into recorded values for hemo~ dynamic measurements. This may have attributed to some of the differences when clinical and hemodynamic subsets did not correlate (see Table 5). The investigator utilized both subjective and objective data when assigning subjects to clinical and hemodynamic subsets. The subjective data may have resulted in some internal bias when assigning subjects to subsets a 1m plications Cardiopulmonary assessments in conjunction with hemodynamic measurements are not routinely performed by nursing 0 If the professional RN were to assume this function on a regular basis the number of fatalities 41 due to left ventricular failure might be reduced. Since the advent of SNP therapy, nursing has been accomplishing the management of SNP therapy on the basis of hemodynamic measurements alone. Nursing has not taken into account the {X)ssibility of equipment malfunction or improper technique while accomplishing hemodynamic measurements, and subsequently used clinical data to expand the data base on which critical judgments are made. The opportunity to improve nursing care is both pos sible and neces sary to improve patient care 0 In clinical settings where hemodynamic monitoring is accomplished expectations of the R N are high 0 Experience and the study results has shown that the highly skilled RN, is capable of and can achieve competence in performing cardiopulmonary assessments and hemodynamic measurements. However, to achieve the desired level of competence there needs to be a planned course of instruction with expected skills to be demonstrated 0 A logical method to provide incentive to learn advanced skills would be a clinical ladder in which the clinical unit defined competencies to be achieved at each leveL The most advanced level could require the RN perform a complete and accurate cardiopulmonary assessment in conjunction with hemodynamic measurement. The RN who achieves this level would then be considered clinically competent to administer and manage patients receiving vasodilator therapy for left ventricular failure due to acute myocardial infarction. ISR: 42 R ecommenda tions The pertinence of clinical data could be increased if the following gUidelines had been included in the methodology: 1) that the physicians who participated utilized the same recording technique as the investigator, and 2) that all RNs accomplished hemodynamic measurements utilizing the same technique 0 These guidelines would have provided to the investigator a more valid and reliable data base of clinical informationo Future studies, embodying these recordings, would provide a core of clinical data useful for determining the extent to which the competent, highly skilled R N is capable of managing patients with left ventricular failure 0 APPENDIX A PHYSICIAN NOTIFICATION Dr" Your cooperation and permission are requested in a study designed to increase the effectiveness of nursing care provided in the coronary care unit" has been contacted and has consented to participate in this study" The study involves the patient receiving a cardiopulmonary assess = ment consisting of auscultation of the heart and lungs with palpation of the trunk and peripheral pulses" The number of assessments conducted will be determined by the severity of the patient's conditiono This study is being conducted by Alfred Be Miller, RN and is being supervised by Dr. Frank Yanowitz, M .. D and Dr" Steven Klausner, MoD" of the Cardiology Department of LDS Hospital This study has been reviewed by the University of Utah Review Committee for Research with Human Subjects and the LDS Hospital Research and Human Rights Committee" These committees have determined that the patient will be at Low or No Risk during the study.. A copy of the study proposal is on file with each committee .. 0 0 Questions can be directed to Alfred B" Miller, RN or Dr. Yanowitz MoDo and Dr Klausner, M"D" 0 Thank you for your cooperation 0 Alfred B" Miller RN Principal Investigator J Permis sion is granted Dr. , denied --------------~ -------------------------------------- ------------- 9 APPENDIX B PATIENT INFORMATION 1. Name 3. -------------------------- 2. Number Age 5. Race -------- 4. Sex 7. Height ----- 8. Allergies 9. Date of AMI ----- 6. Weight __kgo ---------------------------------- 10. Location of AMI -------------------- 11. Enzyme Levels: Normals Date/Time CPK -- LDH -- SGOT 12.. Family History: 130 Chief Complaint: 14. Review of System: 9.0~10600 90.0-21000 10 0=4500 0 APPENDIX C CLINICAL ASSESSMENT DATE/TIME MEDICATIONS: VITAL SIGNS: TREATMENTS/RESPONSE: ASSESSMENT: Subjective Objective Heart Lungs Vessels Skin Assessment Plan APPENDIX D HEMODYNAMIC MEASUREMENTS ca.t.a/!!.::e I 2~O I I 2)0 210 190 ,! 1- 1'70 150 HR BP 1;0 110 90 10 50 )0 7 6 .; 4- CO C! J 2 1 50 I?A SiD t1P~ S"IR ~ JO 20 10 SNP !!Iq;/kg I j I APPENDIX E SUMMARY Subject # 1 Date Time Hemo dlynamlcs HR l 64 60 60 BP 1140/98 ll6/86 140/90 CO CI PA MP\tVP SVR Clinical S1 nl n1 n1 S2 n1 n1 nl S3 0 -0 ! ! 0 S4 0 0 0 Rales + + I + Rhonchi 0 0 0Wheezes lj ~ 5' Output 2:i.iO 17RO 850 Skin Color nl nl n1 Temp warm warm warm -0 Moist 0 0 Dry + + + Mental State Obttmd. ~f____~____4-____~__~____-+____~____~__~____~ Nonnal ~[_+~__~+__~~+__~____~____~__~____~____~_____ Subsets Clin. ~_C~1__~C~1:...-+-~C~1~_ _-I-_ _-I-_--+__-+-__-t-_--t Hemo. ~____~____~____~__~____~____~____~__~____~ 48 Subject # 2 Date Time Hemo dlynamlcs HR I 80 86 86 BP 1160/98 170174 96/74 CO CI I PA MPWP SVR Clinical Sl S2 S3 nl nl nl nl nl nl 0 0' 0 + 0' 0 +LR + R L +R L S4 Rales Rhonchi Wheezes + Output 11873cc Skin +R l612~c I 0' l1520cc ~~f.~ Iwa:~ Iwa:~ r::tt I I I I I I Mental State ~----~----+---~~--~----+---~-----Ir----T----~ Obtund.' Nanna 1 ~.~+L-~~+~~_+~~____~__~____~____.__________~ Subsets Clin. C1 Cl Hemo. I 49 Subject # 4 Date 14/28/7814/28/7814/30/71 Time !0830 . 1200 . 1030 _ Hemodvnamics t HR ;);:) 60 i 58 BP lS4/76 i 124/7C 122/80 CO CI PA MP\VP SVR I Clinical Sl nl nl nl S2 nl nl nl -- I S3 S4 Rales Rhonchi Wheezes Output Skin I I I I r () () (1 () 0 0 I + R T i+ R I +RT 1"'\" n ('5' 0" 0 0 1102 1230 1400 gf.~ Iw:m Iw:~m Iw:~ I Mental State I I I I ~~:~i I + +! + Subsets Clin. Hemo. I ____ Cl ~ ~ I Cl Cl ____~____~__~____~__~~__~____~__~ 50 Subject # 5 Date Time Hemo dlynamlcs HR 54 BP 112./64 CO CI PA MPWP SVR Clinical SI nl S2 nl S3 5' S4 5' Rales 0" Rhonchi 0" Wheezes 0" Output 2~8cc Skin Color nl Temp warm Moist Dry + Mental State Obtund. Normal Subsets Clin: Hemo. '" 48 72 74 110/80 108/78 120/68 I I nl nl nl nl nl nl 5' 5" 5" 5" 5' 5' 0" 0" 0" 0" 0" 0" 0 0 0 i 2714cc t1648cc nl nl nl twarm warm warm + + + ~----~----+---~----~----+---~----~----T---~ + + + + . ~~C~l~~~C~l~~C~l~~C~l__~__-+____~__~____~____~ L ____~____~__~~--~----~--~____~____~--~ 51 Subject # 6 Date Time Herno dlynam lCS HR BP CO CI PA MP\VP SVR Clinical 84 88 80 83 )124/70 88/68 102/80 104/7: I Sl nl nl S2 nl nl nl nl nl nl S3 0 0 n 0 S4 + + + + Rales rt-L R f+- L R + L R H-LR Rhonchi 0 0' 0 0' Wheezes 0 0' 0' 0 Output 7098 3917 3306 Skin ~?~ ~~~01W~cll~~cll:Lcll II i I I II I Mental State Obtund. Normal Subsets 1~--~----~----4-----~---+----+---~I-----r--~ + + + + . . Clin. ~~C~l~~~C~l~__C~l~~C~l__~__-+____~__~____~____~ Herno. ~____~____~__~____~____~__~____~____~__~ 52 Subject # 7 Date 15/3/781 . 0930 Time Hemodynamlcs j 80 HR BP CO CI PA MPWP SVR Clinical 194/60 I Sl I nl nl 0 S2 S3 S4 Rales Rhonchi Wheezes Output Skin I I + + I 0 a ~p ~~l:~n;m~1~I~I-.·~I~I~I~I~I~I Mental State Obtund. Nonnal Subsets Clin. Hemo. II-_.l-!-~--+--4--+--+-+-I-+-----1 ~+~~.~ L. I Cl I __~____~____~__~____~__~_____~____~ 53 Subject #8 Date Time Herno dlynamlcs HR BP CO CI 100 1130J98 I ) I 100 1 94 100 9Q 103 100 100 120/7R' 132/78 104170 100/80 100/70 104/76 104/64 1 PA MPWP SVR Clinical I S1 S3 nl nl 0" S4 0 S2 nl nl nl nl nl nl -0 0 0 + faint + faint + faint - + nl nl 0 faint nl nl nl nl nl nl -0 -0 0 ± faint + faint + faint Rales 0 + + + + + + + Rhonchi I Wheezes + + + + + + Output -2478 1739 1750 1:50 736 1303 1611 Skin cyanotic cyarrOC cyarrOC Ojaroic cyanic cyanotic C)8Jtti.c cyanic Color warm ~l/wrm warm warm rnarm rnarm warm warm Temp Moist + Dry + + + + + + + + Mental State Obttmd. I~ ~ ~ ~ ~ +-__~____~____+-__~ Normal . + + + + + + + + Subsets CUn. C2 C2 C2 C2 C2 C2 C2 C2 I ____ ____ __ ____ ____ I Hemo. :====::========::==========:====:==========:====: 54 Subject # 9 Date Time Hemodvnamics ! HR 120 120 64 88 100 146 82 94 80 BP i124/80 124/72 120/80 98/54 104/68 L04/68 130/80 106/70 L20/80 [ CO CI t PA MPWP SVR Clinical I I I I I S1 nl S2 nl S3 0 S4 () nl nl 0 0 n nl nl 0 n nl nl 0 0" 0 nl nl I nl nl nl nl nl nl nl + 0 + 0 0 0 -00 o nl -0 o. 0 0" ,tRa1es tof' 01' o 0Rhonchi 0 0 0 0 0 0 0 0 0 Wheezes 0 0 0 0 0 0 0 0 0 1401 1334 1550 Output 300 1600 1525 650 1650 Skin nl nl nl nl Color nl nl nl nl nl Temp warm warm warm warm warm warm warm warm warm Moist sli,ght sliQ"ht Dry + + + + + + + Mental State Obtund. ~____~____~__~____~____+-__~____~____+-__~ Normal . + + + + + + + + + Subsets Cl C1 Clin. C1 C1 IC4mildi Cl C3 C2 Cl Hemo. ...1-_-_-_;;;..;_~_-:.-_-_...;;_-_-.... ~_;..;;;_.;;;.;_~...;..;,""",,,,,"::::::::::::::::::::::::::::::~ .... I ss Subject # 10 Date Time H erno dlynamlcs t HR 62 56 68 68 86 BP i94/60 108/66 102/70 104/60 110/70 CO I CI PA MPWP SVR Clinical SI nl nl nl nl nl S2 nl nl nl nl nl S3 0" 0" 0" 0" 0" S4 () 0 0" 0 0" Rales () n~ n 0' n Rhonchi () 0" 0 n 0 Wheezes () () n n n 1300 4130 2300 Output Skin nl nl nl nl nl Color Temp warm warm warm warm warm Moist Dry + + + + + Mental State + I Cl I + I Cl I + + + Cl Cl Cl I I 56 Subject #:11 Date Time Hemo dtynamlcs I HR 70 80 I 93 68 68 BP [22/80 130/80 122/70 90/60 94/66 CO CI PA MP\VP SVR Clinical I S1 S2 S3 n1 n1 n1 n1 n1 n1 n1 n1 n1 n1 '0 0' 0' 6" 6" S4 0' Rales c Rhonchi a Wheezes 6" Output 775 Skin Color n1 Temp warm Moist 6" c c s E () () S0' 6" 6" 6" 6" 1175 1320 300 (pc rtia1 r eport) n1 n1 n1 warm warm warm + Dry 6" 5" 5" + + I n1 warm + + Mental State Obtund. ~____~____~____+-__~____-+____~__~~__~____~ Normal . + + + + + Subsets ain. 1~~C~1~~C~1~t __~C~1~I~C~1~~~C~1-+____~__~~__-+____~ Hemo. ____ ____ _____. ____ ______________ ________ ~ ~ ~ ~ ~ ~ 57 Subject # 12 Date Time Hemo dtynamlcs 88 I HR ,i BP CO CI i 104/70 112/82 110/70 I 100 98 PA MPWP SVR Clinical Sl S2 i ! I nl nl nl nl nl nl S3 0 0 0 S4 Q Q Q I c ct c j 0" 0' 0' Rales Rhonchi Wheezes Output Skin Color 0- 1070 nl warm Temp Moist Dry Mental State Obtund. Normal Subsets Clin. Hemo • + 0- 2100 i rr 1530 nl nl warm warm + + I~----~----~----+---~-----r----+---~~--~----~ . + + + I C1 Cl Cl l..,~_ -_ -_.;:;;;._.:;.._ -.L...,!-_-_...;_;;;.:_=-.-+-_-___ ... ...::_:;.:;_-... +-_-_-_-_-.... -+_-_-_-_-_-... +-_-_-_-_-..... -+-_-_-_-_-.... ~-_-_-_-_-..... -1-_-_-_-_-....... --1 S8 Subject #' 13 Date Time Hemodlynamlcs ) HR 64 64 BP ! 100/74 11l2/82 CO ! CI I 70 80 98/64 104/70 PA MP\VP SVR Clinical I Sl nl S2 nl S3 0 S4 0 Rales 0 Rhonchi 0 Wheezes 0" Output 1400 Skin Color Temp Moist Dry Mental State Obtund. Normal + Subsets Clin. C1 Hemo. nl nl nl _nl nl nl 0 0 0' 0 0 C C- 0 0 0' O' 0 0' 0' 0 1356 I I 1420 1560 I~a~ I;a:~ I~a~ ~~ I I I + + + C1 C1 C1 I 'I I I I I I I 59 Subject #14 Date Time Hemo dlynamlcs HR !60-150 70 54 68 63 65 BP i150/120! 88/62 121/78 100/64 108/81 1100/80 CO i I 3 90 3 39 3 74 4 08 CI 2 Ot) I 1 79 1 97 ? 15 PA J 21/8 46/22 42/20 44/24 MPWP 22 26 13 24 I \ SVR 23 24 I 25 I 25 1 Clinical n1 1 nl SI nl nl nl nl I nl I S2 nl nl nl nl nl S3 a new 5" ~nterm 5" 5" I S4 0 0 0' 0" '0 5" I Rales ct c c 0' I C 0' Rhonchi 0 0' 0' 5" 5" I IT Wheezes 0' f 5" 0 0' 0' 0 Output 1167 990 1815 3366 2800 ! Skin nl Color nl nl nl nl nl Temp warm warm warm warm warm cool Moist slight Dry dry dry dry + + Mental State Obttmd. ~____~____~__-+____~__~~__~____~__-+____~ Normal . + + + + + + Subsets Cl Clin. Cl C4 C2 Cl C2 Hemo. 1-1-_-_-_-_-....1-+_-_-H=3=:~::H=4=::H:..;;..4-_-... -+-_- I _-H:2::::::::::::::::::::::: 60 Subject # 15 Date Time Herno dlynamlcs 63 ! 64 HR 51 ! BP i 118/72 118/82 110/68 CO CI PA MPWP SVR Clinical Sl S2 S3 S4 Rales Rhonchi Wheezes Output Skin I nl nl nl nl nl nl I 0 0 0 0 0 0 0 0 0 I + + I 0 0 0 0 I 2120 1455 1140 ! ! I I ~~~ :~lw:_a:~ :_~:_+:lw:_a:~ :_~:_.:~lw:_a:~ :_~:_~:I= =:~I=_-=_=~:I~:-=_=-=:~I=_-= _-=:~I_=-=_=-=:~I= =_~=:I __ == __ Mental State Obtund. Normal Subsets Clin. Hemo .. C1 C1 C1 __ 61 Subject # 16 16/14/ 16/15/ 16/16/71 Date 78 78 Time i 0600 0800 0815 Hemo dlynamlcs HR 82 92 94 BP 1110/82 106/68 118/70 ! CO CI PA I MPWP SVR Clinical i nl nl S2 nl S3 0 S4 Rales Rhonchi Wheezes Output Skin Color Temp Moist nl nl a 0 0 Q 0 0 0 + + + + n 0 +"*' 2133 1700 2025 dusky dusky dusky warm warm warm Dry Mental State Obtund. I~ Normal . Subsets Clin. nl 1 0 0 a dry dry dry ____+ ____ + ~ C2 +-__~____~____+-__~____~____+-__~ C2 + I ~2 I H~o. ~==~:=~==:~:.=:~:~.=====~====~====:=====:====:====: 62 Subject #17 Date Time Hemodvnamics HR ! 110 96 BP i 98./67 100/69 CO I 4 21 4.32 CI 2.03 2.54 PA 50/20 50/28 MPWP 22 20 SVR 17 19 Clinical SI nl nl S2 nl nl S3 + + S4 Rales H- Q'r()ss +, Rhonchi Wheezes + + Output Skin - gf.~ - I ..... iI i I 1+1+11111111 Mental State Obtund. Normal Subsets ! . + ; I . Clin_!L __~C~4~~C~4~1____~____~__-+____4-__~~__~____i Hemo_ L__nH~4-L~H~2~____~____~__~____~____~__~____~ 63 Subject #18 Date Time Hemo dlynamlcs i 82 90 I 91 HR 92 I 84 BP 112Q/88 1114/86 136/90 L48/98 138/96 CO I I CI I PA MPWP f I SVR Clinical SI I nl nl nl nl nl II 82 nl nl nl nl ! S3 5" 5" 5" 5" snlit 5" 84 0 0' 0" + + Rales 5" 5" 5" + + Rhonchi 0 0 0' 0' 0' Wheezes 0 0 0 0 "0 Output 1105 2500 1000 1475 Skin Color nl nl nl nl nl Temp warm warm warm warm warm Moist 0 0 5" 0 0 Dry + + + + + Mental State Obtund. Normal Subsets Clin. Cl Cl Cl Cl Cl Hemo. I , I 64 Subject # 19 Date Time Hemo dtynamlcs I HR 76 52 82 64 BP 1138/88 124/84 128/88 112/82 CO CI PA MPWP SVR Clinical S1 S2 S3 S4 Rales Rhonchi Wheezes Output Skin Color 1 nl nl nl nl nl n1 nl nl i 0 I 0 0 0 0 0 0 0 L 0' 0' + + + 0 0 '0 0" 0' '0 305 640 460 + ! I 1930 nl nl nl nl Temp warm warm warm warm -0 Moist 0 0" 0 Dry + + + + Mental State Obtund. ~____~____+-__~____~____+-__~____~____+-__~ Normal . + + + + Subsets Clin. C1 C1 C1 Cl Hemo. J.... ...._-_-_.:::::._.=.._~!-_-_~_~_=-.+-_-_-_.;;;:: .. _;.;;;....I-t.:~:~=:=:==:====:====~:====:====: I I I 65 Subject #20 Date Time Hemodvnamics HR ,! 97 76 85 90 70 BP 1114/74 102/60 94/60 105/70 180/10C CO I CI PA i MPWP SVR Clinical Sl nl U1 nl nl S2 S3 0' 0' (5' S4 0' Rales + + Rhonchi 0 0 Wheezes 0 0 Output 1655 425 Skin Color nl nl warm !Warm Temp Moist 0 0 Dry + + Mental State Obtund. Normal Subsets Cl C1 Clin. Heme. nl nl nl nl nl nl i 0' -t- 0' 0 I o + ~+ + "'+ 0 0 0 0 0 0 2240 1185 f ! I , \ 430 nl nl nl warm warm warm - -0 0 + + C31 C2 0 + Cl C3 -- episode of hypotension and 8-12 hrs. Z .; urine output for that period 230 ml for 16 hr s. 66 Subject #21 Date Time Hemodynamics I HR i B:i I 85 BP 1140.11041 J44/102 CO I ! CI I PA ! I MPWP SVR Clinical Sl 1 J I 1 iI split split I S3 split split 5' 0" I S4 + + + S2 Rales 0" Rhonchi 11' Wheezes 11 Output Skin Color nl Temp warm Moist J.L Dry + Mental State I Obtood. Normal Subsets Qin. Hemo. II lL nl warm 11 ± ~----~---4----~----~---r----rl ----r----r--~ . + + . __ __ ~1~C~1~ ~C~34-____~__ ~ ~I --r----T--~ L____-L____~__~~__~----~--~.____~____~--~ -r____ __ 67 Subject # 22 Date Time Herno dlynamics HR 150 f BP i 93/68 CO 4.85 CI 1.98 PA 29/17 MPWP 13 SVR Clinical Sl nl S2 nl S3 + S4 0 Rales + Rhonchi 5" Wheezes 0 Output so Skin Color n1 warm Temp Moist + Dry 0 Mental State Obtund. Normal Subsets Clin. Hemo. 95 107/74 4.48 1.83 34/13 15 18 93 117/79 4.79 1.96 41/17 16 15 85 107/71 4.64 1.9 39/16 15 16 88 110/70 5.61 2.29 43/18 16 14 nl nl nl nl nl nl nl nl nl nl nl nl nl nl nl nl + + + + + + + + 0 0 5" 5" 0' 5" 0 5" t+ 't+ 1'+ + + + + + 5" 5" 0- 5" 0- 0 0 0- 1?O 1 0' RRfl lRO :iSS nl n1 nl warm warm warm 5" 0' + 0 93 92 59 66 108/71 101/66 89/56 89/56 6.26 6.05 5.24 4.75 2.56 2.47 2.1 1.94 41/17 39/12 47/15 48/17 15 12 20 15 12 12 12 13 I 0' 5" 0' + + RJ.O 1qn + SR + 14 nl nl nl nl nl warm warm warm warm warm + + + + + + 0 0 0 0 0 0 68 Subject # 23 Date Time Hemo dlynamlcs 1 HR 90 100 68 93 BP i 136/70 126/70 116/60 110/60 CO CI I PA MP\VP SVR Clinical i I Sl S2 S3 S4 Rales Rhonchi Wheezes Output Skin Color Temp Moist nl nl nl nl nl nl 0 0 0 0 0 0 a a + + 0 0 0 a a a -0 2~513215 nl nl 1800 nl warm warm warm a + Dry Mental State Obtund. Normal Subsets Qin. Hemo. nl nl I 0 1300 nl warm 0 0" 0 + + + I~~~~~~~--+--~~~~~--~----~--~-----r----~--~ + + + + . ~~C~I~~~C~l~__C~l~~C~l__~__~____~____~__~____~ ~ ____~____~__~____~____~__~__________~__~ 69 Subject #24 Date Time H emo dtynamlcs HR ! 86 BP i 94/60 CO I 6 18 CI 2 75 PA 36/18 MPWP 14 SVR 1 :i Clinical SI n1 S2 nl S3 85 80 80 108/71 nO/80 108/74 5 74 2 65 I 34/13 15 l:i I n1 n1 n1 nl nl n1 5" 5" 0' S4 5" 5" 5" 0' Rales + + + + Rhonchi 0 0" \Vheezes 0' 0' 2065 2144 Output Skin nl Color nl nl nl Temp warm warm warm warm Moist 0 + + + Dry 0" 5" 0' + Mental State 23~6 12~OO Obtund. Normal Subsets Clin. Hemo. I I ~~O~~__5"__+-_O __~~O__~____~__~____~____+-__~ . + + + + I C2 C2 C2 C2 :==H::1=:==H:]=:=::=~:::==::::=:=::=:=====:====:====: 70 Subject #25 Date Time Hemo dlynamlcs HR ! 72 100 88 92 104 BP i13RLR2 1112/R2 1112/84 110/80 _96lf> 6 CO I CI PA MPWP I SVR Clinical Sl S2 S3 S4 I nl nl 0 0' Rales + Rhonchi aWheezes 0' Output Skin Color nl Temp warm Moist aDry + Mental State nl nl nl nl nl nl 0 0 nl nl 0' 0 0 + 0 0' + a- a- 0 0 0 aa- + + a- 0 685 5051 3250 2960 nl nl nl nl warm warm warm warm 0 0 0 0 + + + + a- a- a- + + + C2 C1 C1 • 1 I I I 71 Subject #26 Date Time Hemodlynamlcs HR ! 98 BP i 94/62 CO I .'1 R CI 2 4S PA 47/30 MPWP 25 SVR 22 Clinical Sl nl S2 nl S3 + 84 5" + 5" + 76 96 100 99/6;) 96/6.'1 94/6.'1 4.0.'1 ? n 3 R 3 7 2 :; 2 :; 38/28 60/24 54/22 22 19 23 17 18 17 nl nl nl nl nl nl + 5" + 5" + + 5" + 5" + + 5" + 5" + , i I I 1 I I Rales Rhonchi Wheezes Output 140 300 12445 520 Skin Color nl nl nl nl wm/cl wm/cl wm/c} wm/cl Temp + 0 + 0 + 0 + 0 Moist 0 0 0 0 Dry Mental State ~~::~i 1~--;--4--+-5"--~-;--+I-;--~----~--~~--~----+---~ Subsets cun·1 ----:c:::2~-.::c=2_4_--.....:Hc==22::......,..I-H.;:;;:c22=---1-----lI---~--;-----+---1 ____ ________ ___ Hemo. I- ~~H~2~~~H~2~~~~.~~~ ~ ~ ~ 72 Subject # 27 Date Time Hemodlynamics HR ,! 56 56 55 BP ; 110/74 110/70 116/80 CO I CI PA I I MPWP SVR Clinical 1 I Sl nl nl nl S2 nl nl nl S3 0 0 0 S4 + + + + + 0 () () Rales () Rhonchi ;::;Wheezes 2320 Output Skin Color Temp Moist Dry Mental State Obtund. [ Normal + Subsets ..j.. Clin. Hemo. C2 I , -;:; I 1550 Iwa~~ Iwa~~ Iwa~~ I I I I I I [ Q + + C2 C1 I I I I 73 Subject #28 Date Time Hemod namics HR BP CO CI PA MPWP SVR Clinical Sl S2 nl nl nl nl nl nl nl nl nl nl nl i nl i nl nl nl nl nl nl S3 + + + + + + + + + S4 6" 6" 6" 6" 6" 0 6" 0' 6" Rales + + + + + + + + + Rhonchi 0' 6" 6" 6" 6" 0 6" 6" 6" 6" () 0 0" 0" 0 0 6" 1755 1210 Wheezes Output Skin 2011 nl Color warm Temp + Moist Dry Mental State Obrund. Normal 6" Clin. I nl nl nl nl nl nl warm warm warm warm warm warm warm 0 0" 0 0 + + + (} 0 0 + + + + nl nl warm 0 + (} 0 0 0 6" 6" 6" 6" 0 [~----~~~+-~~~~~~--+-~~--~-r----~--~ t + + Subsets Hemo. 0 1510 + + ~I H4 + + I + I + + C2 C2 C2 C2 C2 C21 C2 ~---!---+----;---t___-+-~~---r~~+--~ C21 . HI H3 H4 H2 I HI 74 Subject #29 Date Time Herno dlynamics HR BP CO CI ! 72 I 46 60 160-214 124 72 56 1100/60 102/60 98/70 1~6~( 94/68 l04A)0 98/54 I PA MPWP SVR Clinical Sl S2 S3 S4 Rales Rhonchi Wheezes Output Skin Color Temp I nl nl nl nl nl nl nl nl nl nl nl ! nl ! 0 0 0 0 0 0 + + + + + + + + + + + + 0 0' 0 0' 0 0 0' 0 0' 0' 0' 0 725 1060 1080 600 2170 nl warm Moist 0 0 0 + + + __ I 0 I + I , 0 0' (5' 1230 nl nl nl nl nl nl warm warm warm warm warm warm Dry Mental State I nl nl + + 0 0 0 + + + _____ ~~~~il~ ~~~~~~+-_+~o~~~~~_+~o__~~~~~I ~ ~1----~--~ Subsets Clin. Hemo. 75 Subject # 30 Date Time Hemodynamics HR ~ 115 BP CO CI PA MPWP SVR Clinical 117 118 127 93 li80/114 156/96 147/85 114/76 113/66 2.89 3.26 3.16 1.85 2.32 1.80 2.02 1.96 1.14 1.44 46/15 50/20 35/23 44/23 21 20 20 15 19 42 33 46 37 38 Sl nl nl nl nl S2 nl nl nl nl S3 + + + + S4 0' 000Rales + + + + Rhonchi 00' 0' 0Wheezes n 00' 0" 3422 Output 864 Skin Color nl nl nl nl Temp warm warm warm twarm Moist + + + + Dry 0" 000Mental State Obtund. Normal Subsets CUn. Hemo. nl nl + 0- + 00- 1273 nl warm + 0" I i 76 Subject :# 31 Date Time H emodynamics HR 120 : 120 116 BP 1128./88 150/90 126/90 , CO I CI PA MPWP SVR Clinical S1 S2 S3 S4 Rales Rhonchi Wheezes Output Skin I soUt nl 0' soUt nl ~nlit i nl I 0' I 0" J solit solit split + + 0 j 0 0 0' I IT 0' 0' 1390 I IDI0 1 ! Ef.~ ~wI=!. : a~ i=m!. ::~:l -l~=.!:.a~=. =~m 1 t-1~w: . :; a:~i=m~l=_I~ I" "'= _~-+I=-= =-.:.... _=-= -:-:--tl -=-= _:+1=-= -=-= _:Ir-= -=-= _:-1"= -=-= -=-: "1"1=-= Mental State Obtund. ~I~O'~~~o__+-~o~~____~__~--__~----r-__~____~ Normal ~.~+__~~+__~_+~~____~__~____~________~_____ Subsets Clin. Hemo. ~---...:C2~-4-~C~2---1-_C~1-+-----+---~----t----t_--___t------ . APPENDIX F OPERATIONAL DEFINITIONS Cardiac Output: The amount of blood ejected by the heart expressed in liters/minute .. Cardiac Index: The cardiac output divided by the body surface area, expressed in liters/minute/M2 , used to normalize cardiac output for body size . Pulmonary Artery The pressure in the pulmonary artery, expressed in Pressure: mm Hg" Pulmonary Wedge The pressure in the pulmonary capillary, expressed Pressure: in mm Hg", usually reflective of left atrial pressure .. Systemic Vascular The resistance to blood flow in the systemic system Resistance: throughout the cardiac cycle, calculated as mean arterial pressure - mean right atrial pressure cardiac output . W00 d ' - RAP) and express In ( MAP CO unlts, w hen MAP RAP CO = x 80 it is expressed as dynes sec/CMS . Subsets: Classification of the physiological state of left ventri ~ cular function. Clinical subsets are defined as the data obtained from the history, physical examination and rc'utine laboratory findings.. Hemodynamic subsets are defined using measured hemodynamic parameters such as CO, CI, PAP, and PWP" In the acute patient, clinical and hemodynamic subsets should correlate to justify their use in directing therapeutic decisions. Cardiopulmonary Assessment: Clinical evaluation based on history, physical examina-> tion and routine laboratory findings .. REFERENCES Adams, No R. Reducing the perils 1 976, 75, 66 -74 . intracardiac monitoring. Nursing Alder, J. 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J Studies on the acute cardiovascular effects of intravenous sodium nitroprusside Ameri = can Journal of Cardiology, 1962 ~ ~9 51-590 0 0 Silverman, M. E. A problem oriented approach to coronary care. Hospital and Specialty Practice~ 1971, 380=385. Tanner, G. Heart failure in the MI patient. American Journal of Nursing, 1977, 77 (2), 230.,.234. West, J. B. Pulmonary physiology. Baltimore: Williams and Wilkins 1974, 33-50. 2 81 Winthrope, M. M" Harrison's principles of internal medicine (7th ed"),, New York: McGraw-Hill, 1974, pp. 1075 and 1121. Woods, S" Monitoring pulmonary artery pressures" American Journal of Nursing, 1976, November, 1765-1771" Ziesche, S", & Franciosa, J. A Clinical application of sodium nitroprusside .. Heart and Lung, 1977,.Q (1), 99-103 . 0